Increased platelet aggregation and adhesiveness have been implicated in the pathogenesis of the vascular complications of diabetes mellitus but the basis for this increased function is unknown. The major objective of this study is to evaluate the possibility that alterations in platelet membrane glycoproteins might be responsible. Studies of platelet membrane glycoprotein composition, glycoprotein biosynthesis and non-enzymatic glucosylation of protein in normal and diabetic platelets will be carried out. Correlations will be made with various hematological methods of measuring platelet function.